Abstract
Vanadium(IV/V) compounds have been studied as possible metallopharmaceutical drugs against diabetes mellitus. However, mechanisms of action and toxicological threshold have been tackled poorly so far. In this paper, our purposes were to evaluate the metabolic activity on dyslipidemia and dysglycemia, insulin signaling in liver and adipose tissue, and toxicology of the title compound. To do so, the previously reported bisammonium tetrakis 4-(N,N-dimethylamino)pyridinium decavanadate, the formula of which is [DMAPH]4(NH4)2[V10O28]·8H2O (where DMAPH is 4-dimethylaminopyridinium ion), was synthesized, and its dose-response curve on hyperglycemic rats was evaluated. A Long–Evans rat model showing dyslipidemia and dysglycemia with parameters that reproduce metabolic syndrome and severe insulin resistance was generated. Two different dosages, 5 µmol and 10 µmol twice a week of the title compound (equivalent to 2.43 mg·V/kg/day and 4.86 mg·V/kg/day, resp.), were administered intraperitoneal (i.p.) for two months. Then, an improvement on each of the following parameters was observed at a 5 µmol dose: weight reduction, abdominal perimeter, fatty index, body mass index, oral glucose tolerance test, lipid profile, and adipokine and insulin resistance indexes. Nevertheless, when the toxicological profile was evaluated at a 10 µmol dose, it did not show complete improvement, tested by the liver and adipose histology, as well as by insulin receptor phosphorylation and GLUT-4 expression. In conclusion, the title compound administration produces regulation on lipids and carbohydrates, regardless of dose, but the pharmacological and toxicological threshold for cell regulation are suggested to be up to 5 µmol (2.43 mg·V/kg/day) dose twice per week.
Highlights
Interest in vanadium actions on biological systems has gradually increased, and its physiological relevance has been established in recent years [1, 2]
Hyperglycemic rats induced by alloxan initially showed an average of serum glucose of 300 mg/dL. e V10-DMAP dosages administrated twice a week for one month period produced a decrease in glucose levels depending on the vanadium compound concentration
In the model of dyslipidemia and dysglycemia produced by one-month consumption of diet
Summary
Interest in vanadium actions on biological systems has gradually increased, and its physiological relevance has been established in recent years [1, 2]. Vanadium is the 18th most abundant element in the crust of our planet, even more than zinc (0.019% and 0.008%, resp.). Regarding this occurrence, vanadium is present in the soil, water, and air, in almost all types of ecosystems. Vanadium is present in the soil, water, and air, in almost all types of ecosystems It is absorbed by plants and travels along the food chain up to humans; it is distributed ubiquitously in living organisms [1,2,3]. Metabolism of vanadium in humans and animals has not been fully understood, and evidence is not conclusive as to its importance as a trace element [4]. Metabolism of vanadium in humans and animals has not been fully understood, and evidence is not conclusive as to its importance as a trace element [4]. e estimated daily consumption ranges from 10 to 60 μg depending on a mammal’s diet, but its deficiency in mammals inhibits growth, impairs cellular regenerative functions, and affects thyroid metabolism and bone mineralization, and it causes disturbances in lipid and carbohydrate balance [3,4,5,6].
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